Kidins220 is a transmembrane scaffold protein involved in several types of cancer. The aim of the present study was to examine the role of Kidins220 in tumorigenesis and disease progression of pancreatic cancer. The relevant signalling pathways including EGFR, EMT, and MMP were also investigated. The expression of Kidins220 was examined at the transcript and protein level. The Kidins220 knockdown cell model was established and its influence on cellular functions was determined. Involvement of Kidins220 in tumorigenesis and metastasis was examined in CD1 mice, respectively. The results showed that, reduced Kidin220 expression was associated with tumorigenesis, metastasis, and overall survival of pancreatic cancer. Knockdown of Kidins220 promoted proliferation, colony formation and tumorigenic capacity of pancreatic cancer cells in vitro and in vivo, respectively. Kidins220 regulated pancreatic cancer cell migration through the EGFR/AKT/ERK signalling pathway. Furthermore, enhanced EMT was observed in the pancreatic cancer cell lines with the knockdown of Kidins220, underlying EGFR regulation. Kidins220 also affected cell invasion via MMP1. A reduced expression of Kidins220 was observed in pancreatic cancer, which is associated with disease progression, distant metastasis and poor prognosis. The loss of Kidins220 in pancreatic cancer may contribute to disease progression through the upregulation of EGFR and downstream signalling.Women experience cognitive decline as they age due to the decrease in estrogen levels following menopause. Currently, effective pharmaceutical treatments for age?related cognitive decline are lacking; however, several Traditional Chinese medicines have shown promising effects. Lycium barbarum polysaccharides (LBPs) were found to exert a wide variety of biological activities, including anti?inflammatory, antioxidant and anti?aging effects. However, to the best of our knowledge, the neuroprotective actions of LBP on cognitive impairment induced by decreased levels of estrogen have not yet been determined. To evaluate the effects of LBP on learning and memory impairment in an animal model of menopause, 45 female ICR mice were randomly divided into the following three groups i) Sham; ii) ovariectomy (OVX); and iii) OVX + LBP treatment. The results of open?field and novel object recognition tests revealed that mice in the OVX group had learning and memory impairments, and lacked the ability to recognize and remembt oral LBP treatment may alleviate OVX?induced cognitive impairments by downregulating the expression levels of mRNAs and proteins associated with the TLR4/NF?κB signaling pathway, thereby reducing neuroinflammation and damage to the hippocampal neurons. Thus, LBP may represent a potential agent for the prevention of learning and memory impairments in patients with accelerated aging caused by estrogen deficiency.Following the publication of the above article, an interested reader drew the authors' attention that the data featured in Fig. 1B (for adipogenic differentiation of adipose?derived stem cells) and Fig. 1F (for expression of green fluorescent protein of adipose?derived stem cells) of the above article appeared to have already been published as Fig. https://www.selleckchem.com/products/en460.html 1A (for adipogenic differentiation of adipose?derived stem cells) and Fig. 2D (for expression of green fluorescent protein of adipose?derived stem cells) in the following article Luo L, Lin T, Zheng S, Xie Z, Chen M, Lian G, Xu C, Wang H and Xie L Adipose?derived stem cells attenuate pulmonary arterial hypertension and ameliorate pulmonary arterial remodeling in monocrotaline?induced pulmonary hypertensive rats. Clin Exp Hypertens 37 241?248, 2015. The authors consulted their original data and were able to determine that the duplication of these figure parts had arisen inadvertently during the process of compiling the figure. The revised version of Fig. 1, featuring the corrected data panels for the above?mentioned experiments in Fig. 1B and F, is shown on the next page. The authors confirm that the errors associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this Corrigendum. Furthermore, they apologize to the readership of the Journal for any inconvenience caused. [the original article was published in International Journal of Molecular Medicine 41 51?60, 2018; DOI 10.3892/ijmm.2017.3226].Epilepsy is a common neurological disease that affects more than 50 million people worldwide. Neuro-inflammation plays an important role in epilepsy. Activation of the immune system and an excessive inflammatory response can increase the frequency of seizures and increase the susceptibility to epilepsy. Therefore, anti-inflammatory therapies may have antiepileptic effects. Connexin 43 (Cx43) is a major component of astroglial hemichannels and gap junctions. Gap junctions are important for the direct exchange of substances and information between cells, as well as regulating the neuroinflammatory response, changing neuronal excitability, neuronal apoptosis, and synaptic remodeling. Cx43-mediated gap junction pathway can be crucial in epilepsy-induced neuroinflammatory cascades. Further, pro-inflammatory cytokines may in turn directly affect the expression of the Cx43 protein in astrocytes. Therefore, examining the association between neuroinflammation and epilepsy can be instrumental in uncovering the pathogenesis of epilepsy, which can lead to the development of novel and more effective antiepileptic drugs.Intracerebral hemorrhage (ICH) has the highest mortality rate of all stroke subtypes but an effective treatment has yet to be clinically implemented. Transforming growth factor?β1 (TGF?β1) has been reported to modulate microglia?mediated neuroinflammation after ICH and promote functional recovery; however, the underlying mechanisms remain unclear. Non?coding RNAs such as microRNAs (miRNAs) and competitive endogenous RNAs (ceRNAs) have surfaced as critical regulators in human disease. A known miR?93 target, nuclear factor erythroid 2?related factor 2 (Nrf2), has been shown to be neuroprotective after ICH. It was hypothesized that TGF?β1 functions as a ceRNA that sponges miR?93?5p and thereby ameliorates ICH injury in the brain. Short interfering RNA (siRNA) was used to knock down TGF?β1 and miR?93 expression was also pharmacologically manipulated to elucidate the mechanistic association between miR?93?5p, Nrf2, and TGF?β1 in an in vitro model of ICH (thrombin?treated human microglial HMO6 cells). Bioinformatics predictive analyses showed that miR?93?5p could bind to both TGF?β1 and Nrf2.